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NROSCI 0080: LECTURE 15
what was the average life span in 1900
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50years |
what is the average life span now
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76 for men
81 for women
~50% increase
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what new epidemic has emerged
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age related dementia (impaired memory and cognitive ability)
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what is the principle goal of aging research
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to maintain and enhance quality of life in old age (not lengthening our life span)
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why do behaviors start slowing down when we get old
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ability to do well in timed task may diminish; if there are no time constraints, there will usually be no deficit
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what typical brain changes are observed in people after ~60
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decreased brain weight, populations of neurons decreased in number, decline in amounts of some neurotransmitters, decline in amounts of some neurotransmitters
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what suggests that we would all eventually get dementia if we lived long enough?
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the frequency of dementia within the population increases markedly with age
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molecular mechanisms of aging hypothesis
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since most CNS neurons stop dividing before birth, most neurons a person has are as old as that person (DNA is not that old tho bc it is replenished)
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when does the rate of neural death begin to increase
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60-70 year mark
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what happens to the brain after age 65 and beyond
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the size and weight of the brain diminishes due to increased rate of neuron loss
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"wear and tear"
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a general hypothesis of why the neuron death increases in old age
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what happens when DNA gets old?
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random damage and wear and tear causes DNA to make proteins that don't work because they are made incorrectly or may even be toxic
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memory loss
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the hippocampus plays a crucial role in learning and memory
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why do hippocampal neurons die?
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they are particularly susceptible to reduced blood flow which occurs often in the older brain
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what affect does stress have on hippocampal neurons
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stress increases glucocortisoids which act throughout the body and hippocampal neurons are extremely sensitive and can die with prolonged high levels of glucocorticoids
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death of hippocampal neurons ____ but does not ____
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contributes to memory loss, produce dementia
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autopsy results of dementia
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shrunken cortex, amyloid plagues, neurofibrillary tangles
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alzheimers disease
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most common cause of age related dementia
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dementia |
general term describing the global loss of higher cortical functions, especially memory, personality, and language
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what is dementia caused by
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any process that interferes with cortical function (stroke, infectious disease, hydrocephalus, malnutrition, and toxins)
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what percentage dementia is caused by alzheimers disease
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50 (25 due to vascular disease including stroke)
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who is alzheimers disease named after
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alois alzheimer
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how many nursing home beds are occupied by alzheimers patients?
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1/3rd
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what is alzhemers disease caused by
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neuronal death in hypothalamus and brain stem
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AD is especially noted for the loss of neurons in the ___
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telencephalon-basal forebrain
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nucleus basalis
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cholinergic neurons
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tacrine |
first FDA approved drug for combating cognitive losses in AD
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what does tacrine do?
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slows breakdown of acetylcholine in brain (combats acetylcholinesterase) but eventually stops working because target neurons for ACh are dying
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what is severely degenerated in Ad patients?
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hippocampus and neocortex, especially the association cortex of frontal and temporal lobes
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what does a thinning of the cortex in AD patients cause?
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widening of the gyri
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why do neurons die in alzheimers disease patients?
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this is still unknown
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where is there a prominent death of neurons in AD patients
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basal forebrain
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what are the brains of AD patients full of?
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plagues and tangles
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plagues
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accumulation of a large unprocessed form of beta amyloid protein (a-beta) which is usually present in a smaller cleaved form and the function is unknown
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what is a beta made of primarily and when is it activated?
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microglial cells and it is activated during inflammatory responses
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what protein usually helps to degrade abeta?
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A2M usually shuttles abeta into neurons where it is broken down by lysosomes but it is not present in alzheimers patients
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neurofibrillarytangles
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intracellular tangle of cytoskeletal elements in dead neurons
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pittsburgh compound
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amyloid plagues can be viewed in a pet scan using "pittsburgh compound"
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is AD hereditary?
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not in most cases
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how are amyloid plagues related to the cause of AD
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responsible genes that are transmitted lead to an excessive accumulation of amyloid plagues so its possible that they are the underlying cause
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what are some things that might prevent AD?
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vaccination against A-beta or estrogen
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microglial cell
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scientists believe that excess big form of beta amyloid (abeta) are made by microglial cells
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glia |
normally function to provide nutritional and physical support to neurons
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when are glia cells activated
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when neurons are dying -- part of the inflammatory reaction
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treatment of rheumatoid arthritis
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treated with long term anti-inflammatory drugs that reduce the glial reaction to dying neurons (especially low rates of alzheimers disease)
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stroke |
can be thought of as a "brain attack"
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what are the two major types of stroke?
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ischemia and hemorrhage
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ischemia
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more mild and treatable stroke damage results from lack of blood flow to the brain, usually due to a clot
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tissue plasminogen activator
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treatment for ischemic strokes (within three hours) that breaks up clots and allows return of normal blood flow to the affected region
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hemorrhage
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more severe and less treatable stroke damage results from a burst vessel bleeding into the brain, usually accompanied by ischemia in "downstream" areas that don't receive their normal blood supply
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diaschisis |
neural shock -- caused by an accumulation of symptoms caused by blood flow being cut off in the brain
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what happens when blood supply to the brian is cut off
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changes in pH, massive release of glutamate which leads to glutamate gated channels being left open and Ca+ is let into cells too much and this causes toxic effects
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treatments for stroke damage
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antioxidants and other neuroprotective drugs to counteract toxic effects
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hemispatial neglect
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strokes often occur in one hemisphere
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